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Syracuse, NY
Dr. Lenox is associated with the Division of Pulmonary and Critical Care Medicine, SUNY Upstate Medical University Hospital.
Correspondence to: Robert J. Lenox, MD, FCCP, Division of Pulmonary and Critical Care Medicine, SUNY Upstate Medical University Hospital, 750 E Adams St, Syracuse, NY 13210
Over the last several decades, progress in the treatment of bronchogenic lung cancer has been disappointing. Lung cancer remains the number one cancer killer in the United States. Lung cancer kills more US citizens than colon cancer, breast cancer, and prostate cancer combined.1 Although most cases of lung cancer could be prevented, the treatment of lung cancer is often disappointing.
New modalities, new drugs, and new methods with which to test the utility of new approaches are needed. In the study of infection, laboratory and animal models have proven invaluable. In the study of human cancer, the efficacy of new treatment ideas in various cell lines can be investigated. This provides preliminary useful information, but it does not provide information on the effectiveness of the agent or agents in the prevention of death or metastasis. Such methods also do not provide us with data about toxicity or tissue penetration. These issues can be studied in human subjects, but such studies are expensive, time consuming, and of potential risk to subjects. An animal model of human lung cancer may accelerate the investigation of new treatment ideas. This approach allows a new agent or idea to be used alone or in combination with various other agents, in rapid succession and in a relatively inexpensive manner.
In this issue of CHEST (see page 1248), Tanaka et al use severe combined immunodeficiency (SCID) mice to develop an animal model of human pulmonary metastatic lung cancer. Non-small cell lung cancer cells (EBC-1) were injected into the flank of SCID mice. The animals soon developed metastatic pulmonary nodules. The tumor used is a human bronchogenic epidermoid carcinoma. It produces neutrophil elastase. Staining for neutrophil elastase confirmed that the metastatic nodules were the same tumor as the tumor implanted in the animals flank. These pulmonary metastatic nodules were evident by week 7. Surgical removal of the flank tumor at week 3 or at week 5 did not prevent the formation of metastatic pulmonary nodules in any of the mice. Blood samples obtained 3 weeks after implantation revealed human ß-actin messenger RNA. This confirmed the presence of metastasis as early as 3 weeks and explained the failure of surgical removal in the prevention of the spread of the human lung cancer.
With this model, it would be possible to investigate the role of traditional chemotherapeutic agents in various combinations in the hopes of finding the best approach to traditional treatment of nonresectable lung cancer. It also gives us a model to investigate neoadjuvant drugs, as well as a method to investigate new ideas in the treatment of lung cancer. Indeed, Inada et al2 have already used this model to investigate a neutrophil elastase inhibitor in the treatment of this same cancer cell line (EBC-1). Other human bronchogenic carcinoma cell lines, or any other malignant cell line, could be investigated using this SCID model.
There are limitations to this model. A major limitation is the lack of an effective immune response in SCID mice. An organism’s immune response may play an important role in the cure of bronchogenic carcinoma. The effectiveness of a given treatment, particularly if it enhances the organism’s immune response to the tumor, cannot be investigated. In addition, the model is a mouse model, and whatever approach the model suggests as being useful will need to be tested in a well-controlled human study.
Nevertheless, Tanaka et al are to be commended for developing this model. It should prove useful in our battle against this unrelenting foe. Such a model might increase the speed with which many new ideas can be investigated. In the meantime, it is most important to do what would have the greatest impact on curbing the desolation caused by lung cancer. It is essential that more be done to prevent this disease. The battle at this time can be most effectively influenced by decreasing the smoking of cigarettes and other tobacco products. It is incumbent that all be done that can be done to prevent and to treat new cases of lung cancer. It is also important that the search for novel agents and methods continue unabated. Without progress along all of these lines, progress against the leading cancer killer will continue to be disappointing.
References
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